Biologists delay the aging process by 'remote control'

September 8, 2014, University of California, Los Angeles
Activating a gene called AMPK in the nervous system induces the anti-aging cellular recycling process of autophagy in both the brain and intestine. Activating AMPK in the intestine leads to increased autophagy in both the intestine and brain. Matthew Ulgherait, David Walker and UCLA colleagues showed that this 'inter-organ' communication during aging can substantially prolong the healthy lifespan of fruit flies. Credit: Matthew Ulgherait/UCLA

UCLA biologists have identified a gene that can slow the aging process throughout the entire body when activated remotely in key organ systems.

Working with fruit flies, the life scientists activated a gene called AMPK that is a key energy sensor in cells; it gets activated when cellular energy levels are low.

Increasing the amount of AMPK in ' intestines increased their lifespans by about 30 percent—to roughly eight weeks from the typical six—and the flies stayed healthier longer as well.

The research, published Sept. 4 in the open-source journal Cell Reports, could have important implications for delaying aging and disease in humans, said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research.

"We have shown that when we activate the gene in the intestine or the nervous system, we see the is slowed beyond the organ system in which the gene is activated," Walker said.

Walker said that the findings are important because extending the healthy life of humans would presumably require protecting many of the body's from the ravages of aging—but delivering anti-aging treatments to the brain or other key organs could prove technically difficult. The study suggests that activating AMPK in a more accessible organ such as the intestine, for example, could ultimately slow the aging process throughout the entire body, including the brain.

Humans have AMPK, but it is usually not activated at a high level, Walker said.

"Instead of studying the diseases of aging—Parkinson's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease, diabetes—one by one, we believe it may be possible to intervene in the aging process and delay the onset of many of these diseases," said Walker, a member of UCLA's Molecular Biology Institute. "We are not there yet, and it could, of course, take many years, but that is our goal and we think it is realistic.

"The ultimate aim of our research is to promote healthy aging in people."

The fruit fly, Drosophila melanogaster, is a good model for studying aging in humans because scientists have identified all of the fruit fly's genes and know how to switch individual genes on and off. The biologists studied approximately 100,000 of them over the course of the study.

Lead author Matthew Ulgherait, who conducted the research in Walker's laboratory as a doctoral student, focused on a cellular process called autophagy, which enables cells to degrade and discard old, damaged cellular components. By getting rid of that "cellular garbage" before it damages cells, autophagy protects against aging, and AMPK has been shown previously to activate this process.

Ulgherait studied whether activating AMPK in the flies led to autophagy occurring at a greater rate than usual.

"A really interesting finding was when Matt activated AMPK in the nervous system, he saw evidence of increased levels of autophagy in not only the brain, but also in the intestine," said Walker, a faculty member in the UCLA College. "And vice versa: Activating AMPK in the intestine produced increased levels of autophagy in the brain—and perhaps elsewhere, too."

Many neurodegenerative diseases, including both Alzheimer's and Parkinson's, are associated with the accumulation of protein aggregates, a type of cellular garbage, in the brain, Walker noted.

"Matt moved beyond correlation and established causality," he said. "He showed that the activation of autophagy was both necessary to see the anti-aging effects and sufficient; that he could bypass AMPK and directly target ."

Walker said that AMPK is thought to be a key target of metformin, a drug used to treat Type 2 diabetes, and that metformin activates AMPK.

Explore further: Boosting 'cellular garbage disposal' can delay the aging process, research shows

Related Stories

Boosting 'cellular garbage disposal' can delay the aging process, research shows

May 6, 2013
(Medical Xpress)—UCLA life scientists have identified a gene previously implicated in Parkinson's disease that can delay the onset of aging and extend the healthy life span of fruit flies. The research, they say, could ...

AMPK amplifies Huntington's disease

July 18, 2011
A new study describes how hyperactivation of AMP-activated protein kinase (AMPK) promotes neurodegeneration in Huntington's disease (HD). The article appears online on July 18, 2011, in The Journal of Cell Biology.

Recommended for you

Human 'chimeric' cells restore crucial protein in Duchenne muscular dystrophy

March 16, 2018
Cells made by fusing a normal human muscle cell with a muscle cell from a person with Duchenne muscular dystrophy —a rare but fatal form of muscular dystrophy—were able to significantly improve muscle function when implanted ...

Team develops 3-D tissue model of a developing human heart

March 16, 2018
The heart is the first organ to develop in the womb and the first cause of concern for many parents.

Genetic variant discovery to help asthma sufferers

March 16, 2018
Research from the University of Liverpool, published today in Lancet Respiratory Medicine, identifies a genetic variant that could improve the safety and effectiveness of corticosteroids, drugs that are used to treat a range ...

Researchers say use of artificial intelligence in medicine raises ethical questions

March 15, 2018
In a perspective piece, Stanford researchers discuss the ethical implications of using machine-learning tools in making health care decisions for patients.

Study identifies potential drug for treatment of debilitating inherited neurological disease

March 15, 2018
St. Jude Children's Research Hospital scientists have demonstrated in mouse studies that the neurological disease spinal bulbar muscular atrophy (SBMA) can be successfully treated with drugs. The finding paves the way for ...

Clearing clumps of protein in aging neural stem cells boosts their activity

March 15, 2018
Young, resting neural stem cells in the brains of mice store large clumps of proteins in specialized cellular trash compartments known as lysosomes, researchers at the Stanford University School of Medicine have found.


Adjust slider to filter visible comments by rank

Display comments: newest first

2 / 5 (1) Sep 08, 2014
'promoting healthy aging' -> promoting aging,
Sep 15, 2014
This comment has been removed by a moderator.

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.